The experiment confirmed that converting the two amino acids to non-functional counterparts did inhibit ECP’s ribonuclease activity.

[14] Studies show that ECP, along with other RNases including EDN, had been reported to induce apoptosis in cells.

[15] Increases in chromatin condensation, sub-G1 population, PARP cleavage, and DNA fragmentation indicate that ECP induces apoptosis in human bronchial epithelial (BEAS-2B) cells.

ECP is one of the four highly basic proteins that enter the surrounding tissues when activated eosinophils degranulate.

[18] ECP concentrations in plasma and other body fluids increase during inflammatory reactions marked by activated eosinophils.

In seasonal asthmatic patients, ECP measurement reflected changes in disease activity throughout the year.

The late phase typically occurs several hours after exposure, upon which eosinophils accumulate in the bronchus and release granule proteins that cause bronchial irritability.

[21] Serum ECP measurement for assessing asthma severity, monitoring therapy, and indicating severity of certain inflammatory skin conditions present an advantage over subjective clinical measures that are prone to inconsistencies due to broad variability of individual investigator and patient assessments, especially in young children.